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Ischemic optic neuropathy occurred in a patient following liposuction. Perioperative anemia and hypotension may be the cause of this complication. Correction of anemia with transfusion improved the hemoglobin and hematocrit but the right eye remained blind. Liposuction should be added to the list of the surgical procedures that may produce ischemic optic neuropathy as an isolated complication.

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A patient with advanced AIDS presented with right conjugate gaze palsy and impaired adduction on left gaze (the one-and-a-half syndrome). The responsible pontine lesion involved the ipsilateral abducens nucleus and the adjacent medial longitudinal fasiculus (MLF), as demonstrated by magnetic resonance imaging (MRI). Tuberculosis (TB) was the etiology of the brainstem lesion. The patient had complete recovery after anti-tuberculosis treatment. The nuclear location of the tuberculoma is unusual and the reversal of this neuro-ophthalmologic syndrome is noteworthy.

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We report a case of tuberculum sellae meningioma with optic tract edema. Contrary to a prior report on this topic, edema along the optic tract is not only seen in craniopharyngiomas but may be seen (although rarely) in other common parasellar tumors, as in our case of a tuberculum sellae meningioma. The pathogenesis of this edema in meningioma is controversial.

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The clinical course of four patients with visual loss in the postpartum period due to acute optic neuritis is described. Factors that disclosed the underlying etiology and expression of disease are discussed. The clinical records of four women examined and managed for visual loss after uncomplicated pregnancies and term deliveries were reviewed. Neurodiagnostic examination, treatment modalities, and outcomes were assessed. These four women with varied and confounding medical histories, all with optic neuropathy, eventually were demonstrated to harbor demyelinating disease. Although visual loss in the postpartum period evokes differential diagnostic considerations, the authors' experience suggests that puerperal immune-mediated changes are responsible for activation of optic neuritis associated with relapsing multiple sclerosis.

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A patient with typical pituitary apoplexy with documented intralesional hemorrhage and spontaneous resolution is presented. There was no evidence of a tumor at a 3-month follow-up.

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A patient with generalized inflammatory polyneuropathy and facial diplegia was studied with magnetic resonance imaging. Multiple cranial nerves showed signal enhancement without sensory or motor dysfunction.

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A 42-year-old woman with a 6-year history of diabetes insipidus and progressive hypersomnolence presented with visual loss. Neuroimaging showed infiltration in the hypothalamus, the optic nerve, and the chiasm, as well as multiple lesions in other areas of the brain parenchyma. Biopsy showed Langerhans cell histiocytosis. This is an unusual presentation of Langerhans cell histiocytosis, involving the visual pathways without manifestations outside of the central nervous system. The differential diagnosis and the magnetic resonance imaging findings will be discussed.

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OBJECTIVE: To determine the incidence of positive neuroradiologic studies in consecutive patients with glaucoma associated with normal intraocular pressure and to compare the psychophysical and clinical characteristics of these eyes with eyes with disc cupping associated with intracranial masses. DESIGN: Retrospective case-controlled study. PARTICIPANTS: Fifty-two eyes of 29 patients with glaucoma associated with normal intraocular pressure and 44 eyes of 28 control patients with compressive lesions were reviewed. INTERVENTION: The medical records of consecutive glaucoma patients with normal intraocular pressure who underwent brain magnetic resonance imaging or computed tomography scanning as part of a diagnostic evaluation between January 1, 1985, and July 1, 1995, were reviewed. A masked reading of optic nerve photographs and visual fields was performed by one observer. A similar analysis was performed on a control group of consecutive patients with nonglaucomatous optic nerve cupping with known intracranial mass lesions. MAIN OUTCOME MEASURES: The neuroradiologic findings, clinical characteristics, optic nerve head appearance, and patterns of visual field loss were compared between groups. RESULTS: None of the patients diagnosed with glaucoma had neuroradiologic evidence of a mass lesion involving the anterior visual pathway. Compared to control subjects, patients with glaucoma were older (P = 0.0001), had better visual acuity (P = 0.002), greater vertical loss of neuroretinal rim tissue (P = 0.0001), more frequent optic disc hemorrhages (P = 0.01), less neuroretinal rim pallor (P = 0.0001), and more nerve fiber bundle visual field defects aligned at the horizontal midline (P = 0.0001). Visual acuity less than 20/40, vertically aligned visual field defects, optic nerve pallor in excess of cupping, and age younger than 50 years were 77%, 81%, 90%, and 93% specific for nonglaucomatous cupping associated with compressive lesions, respectively. CONCLUSIONS: Anterior visual pathway compression is an uncommon finding in the neuroradiologic evaluation of patients with a presumptive diagnosis of normal-tension glaucoma. Younger age, lower levels of visual acuity, vertically aligned visual field defects, and neuroretinal rim pallor may increase the likelihood of identifying an intracranial mass lesion.

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We report two patients with unique homonymous hemianopias from occipital lobe infarctions. One patient had vertical meridian sparing, and the other displayed horizontal meridian sparing. MRI correlation with the visual field defects confirmed that the vertical hemianopic meridian was represented along the border of the calcarine lips, and the horizontal meridian lies at the base of the calcarine banks deep within the calcarine fissure.

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A 66-year-old woman presented with a 3-year history of predominantly right-sided blepharospasm and a 1-year history of progressive predominantly left-sided hemiparkinsonism manifested by a left upper extremity resting tremor and left-sided bradykinesia. Magnetic resonance imaging of the brain revealed a large right mesencephalic cyst with mass effect. Positron emission tomography revealed bilateral striatal hypometabolism consistent with nigrostriatal dopaminergic dysfunction. The association of predominantly ipsilateral blepharospasm and predominantly contralateral hemiparkinsonism is very rare, and its association with a posterior fossa space-occupying lesion has been reported only once. This is the second report of such an association and the first description of adult-onset symptomatology.

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Cutaneous carcinomas of the face, and some nasopharyngeal carcinomas, may present with facial dysesthesias and/or facial nerve palsies in the absence of visible masses. Even with frank ophthalmoplegia, occult tumors that present in this matter may elude detection, for which reason specific diagnostic studies must be employed. We report seven cases of trigeminal nerve infiltration by occult tumors (five squamous cell carcinomas, one basal cell carcinoma, and one adenoid cystic carcinoma), and outline the clinical course, diagnostic investigations, and the subsequent management of these patients. The importance of establishing an early diagnosis before the tumor has transgressed the basal foramina is emphasized, as tumor infiltration of the cavernous sinus carries a more guarded prognosis. The use of magnetic resonance imaging to identify involved peripheral nerve branches that may then be biopsied is suggested. The patho-physiological mechanisms of neurotropic spread of tumor are reviewed.

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The objective of the study was to determine the efficacy of optic nerve sheath fenestration (ONSF) in eyes with progressive visual or field loss in pseudotumor cerebri in spite of medical therapy with oral Diamox. Visual data on 29 eyes of patients with pseudotumor cerebri who underwent ONSF at Bascom Palmer Eye Institute from 1987 to 1995 were studied retrospectively. These patients had progressive visual loss despite medical therapy. Visual acuity and fields were compared before and after surgery (within 1 and 6 months). During a mean follow-up of 15.7 months (range, 1-50 months), visual acuity improved in four eyes (14%), was unchanged in 22 (76%) eyes, and worsened in three (10%) eyes. Visual fields improved in 10 (48%) eyes, remained unchanged in eight (38%) eyes, and worsened in three (14%) eyes (six were lost in long-term follow-up). There were four repeat surgeries in which vision was lost in one eye. Data from these patients indicate that ONSF improves or protects visual function in patients with pseudotumor cerebri who experience deteriorating visual acuity and fields in spite of medical therapy.

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BACKGROUND: Controversy exists regarding the cortical representation of the foveal region in man. The most plausible explanation for foveal sparing in homonymous hemianopia is dual blood supply to the occipital pole. However, bilateral cortical representation has also been suggested. OBJECTIVE: To determine the representation of the foveal region in the primary human visual cortex. DESIGN: A case series correlating magnetic resonance imaging to the visual field defects of 6 patients with occipital lobe injuries. RESULTS: Four patients with foveal-sparing hemianopic defects demonstrated unilateral sparing of the posterior occipital cortex. In contrast, 2 patients with central homonymous defects showed isolated involvement of the posterior pole. One patient also demonstrated 5 degrees of field sparing along the horizontal meridian. CONCLUSIONS: On the basis of correlating the findings of magnetic resonance imaging and visual field defects in patients with occipital lobe injury, we conclude that the foveal region is unilaterally represented in the primary human visual cortex and that a major portion of the striate cortex is dedicated to the central 10 degrees of vision. The horizontal meridian of the visual field is represented deep within the calcarine banks at the fissure base.

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A 15-year-old boy had onset of unilateral facial weakness. A few days later, he experienced mild vertigo, double vision, and headache. Examination confirmed a peripheral right seventh nerve weakness in addition to an internuclear ophthalmoplegia. The neurologic features suggested a pontine glioma. A T2-weighted MRI scan revealed demyelinating lesions in the pons and in several areas of the cerebrum, including the periventricular region. Subsequent history revealed that he had been diagnosed with Lyme arthritis 7 years earlier while living in Connecticut. The radiographic studies favored a diagnosis of multiple sclerosis. However, studies of blood and cerebrospinal fluid established a diagnosis of Lyme neuroborreliosis.

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PURPOSE: We examined a 28-year-old woman who developed incongruous binasal and bitemporal visual field defects one week after having a febrile gastroenteritis characterized by severe diarrhea while traveling in Mexico. METHODS: The patient was treated with intravenous methylprednisolone sodium succinate, 1 g daily for three days, followed by an eight-week course of oral prednisone. RESULTS: Neuroradiologic examination demonstrated bilaterally increased signal intensity within the lateral geniculate bodies. Cerebrospinal fluid analysis disclosed isolated protein increase. CONCLUSION: Severe diarrhea may be associated with an aseptic bilateral lateral geniculitis resulting in hourglass-shaped visual fields. Corticosteroid therapy may provide mild improvement.

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PURPOSE: Severe vistral acuity loss associated with pseudotumor cerebri is usually caused by chronic optic disk edema or a retinal abnormality. METHODS: We treated a women, with known pseudotumor cerebri treated with a lumboperitoneal shunt, who developed acute pallied optic disk swelling and visual acuity of R.E.: no light perception and L.E.: 20/70 in association with lumboperitoneal shunt failure. There were no contributory retinal lesions. RESULTS: The patient underwent optic nerve sheath fenestration and lumboperitoneal shunt revision. Visual acuity improved to 20/20 in both eyes. The papilledema resolved. CONCLUSION: The severe sudden visual loss was attributed to axoplasmic stasis and optic nerve ischemia associated with a sudden rise in intracranial pressure.

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Traumatic chiasmal neuropathy results from injury to the face, sphenoid and clivus. Its pathogenesis remains enigmatic. Because of its close relationship to the pituitary gland, hypothalamus and internal carotid artery, a neuro-ophthalmic evaluation and imaging is needed in such cases. We present a patient who developed traumatic chiasmal syndrome after an automobile accident. Computed tomographic scan showed fracture of the sella turcica. A carotid angiography showed a traumatic pseudoaneurysm of the internal carotid at the base of the skull.

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